Figure 1. Pathways of CeO₂ NPs-induced cell death in primary human monocytes. CeO₂ NPs induce apoptosis involving mitochondrial damage (loss of membrane potential, activation and mitochondrial relocation of BAX) and apoptosis-inducing factor, mitochondrion-associated, 1 (AIFM1) induction. Modulation of autophagic events (increased LC3B-stained autophagic vesicles, monodansylcadaverine-stained autophagosomes/autolysososmes and increased lysosomal contents) decease the cytotoxicity and apoptosis of monocytes. Pharmacological inhibition of TP53 results in an increase in autophagic events, while apoptosis remains unchanged.